RESUMO
The etiology of lactic acidosis can potentially be misleading, especially in a critically ill patient with malignancy. Type B lactic acidosis represents a rare and often lethal complication of malignancy. When differentiating the types of lactic acidosis, Type A is due to marked tissue hypoperfusion and Type B is due to causes in the setting of a normal perfused state. We report the case of a 56-year-old male with newly diagnosed poorly differentiated neuroendocrine metastatic carcinoma and renal cell carcinoma who presented with a decreased level of consciousness and appetite. The patient was started on a sepsis protocol from an initial intensive care unit (ICU) admission. Broad spectrum antibiotics were initiated, and despite management, his mentation and respiratory status worsened, leading to intubation and mechanical ventilation. The patient continued to have elevated lactic acid and white count levels throughout the hospital course. After extensive workup and an ICU stay of 16 days, a decision was made to pursue comfort care measures and the patient passed away shortly thereafter. The patient's persistently elevated lactic acidosis may have resulted from the inherent malignancy. The literature mentions glycolysis with enhanced metabolism as a proposed mechanism. One theory states that these changes enable cancer cells to acquire and metabolize nutrients in a way that favors proliferation over efficient adenosine triphosphate (ATP) production, resulting in elevations of lactate production. Patients presenting to the ICU with elevated lactic acid levels need to be thoroughly worked up for all potential causes. In our case, the underlying malignancies likely caused the persistently elevated lactic acidosis, despite subtherapeutic treatment and resuscitative measures.
